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The molecules: mechanisms of arterial vasodilatation observed in the splanchnic and systemic circulation in portal hypertension.
J Clin Gastroenterol. 2007 Nov-Dec; 41 Suppl 3:S288-94.JC

Abstract

A hyperdynamic splanchnic and systemic circulation is typical of cirrhotic patients and has been observed in all experimental forms of portal hypertension. The hyperdynamic circulation is most likely initiated by arterial vasodilatation, leading to central hypovolemia, sodium retention, and an increased intravascular volume. Arterial vasodilatation is regulated by a complex interplay of various vasodilator molecules and factors that influence the production of those vasodilator molecules. Nitric oxide (NO) has been recognized as the most important vasodilator molecule that mediates the excessive arterial vasodilatation observed in portal hypertension. The aims of this review are (1) to categorize NO synthase isoforms involved in NO overproduction; (2) to explain the mechanisms of endothelial NO synthase up-regulation; and (3) to summarize other molecules involved in the arterial vasodilatation.

Authors+Show Affiliations

Section of Digestive Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. yasuko.iwakiri@yale.edu

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

17975478

Citation

Iwakiri, Yasuko. "The Molecules: Mechanisms of Arterial Vasodilatation Observed in the Splanchnic and Systemic Circulation in Portal Hypertension." Journal of Clinical Gastroenterology, vol. 41 Suppl 3, 2007, pp. S288-94.
Iwakiri Y. The molecules: mechanisms of arterial vasodilatation observed in the splanchnic and systemic circulation in portal hypertension. J Clin Gastroenterol. 2007;41 Suppl 3:S288-94.
Iwakiri, Y. (2007). The molecules: mechanisms of arterial vasodilatation observed in the splanchnic and systemic circulation in portal hypertension. Journal of Clinical Gastroenterology, 41 Suppl 3, S288-94.
Iwakiri Y. The Molecules: Mechanisms of Arterial Vasodilatation Observed in the Splanchnic and Systemic Circulation in Portal Hypertension. J Clin Gastroenterol. 2007 Nov-Dec;41 Suppl 3:S288-94. PubMed PMID: 17975478.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The molecules: mechanisms of arterial vasodilatation observed in the splanchnic and systemic circulation in portal hypertension. A1 - Iwakiri,Yasuko, PY - 2007/12/6/pubmed PY - 2008/2/7/medline PY - 2007/12/6/entrez SP - S288 EP - 94 JF - Journal of clinical gastroenterology JO - J Clin Gastroenterol VL - 41 Suppl 3 N2 - A hyperdynamic splanchnic and systemic circulation is typical of cirrhotic patients and has been observed in all experimental forms of portal hypertension. The hyperdynamic circulation is most likely initiated by arterial vasodilatation, leading to central hypovolemia, sodium retention, and an increased intravascular volume. Arterial vasodilatation is regulated by a complex interplay of various vasodilator molecules and factors that influence the production of those vasodilator molecules. Nitric oxide (NO) has been recognized as the most important vasodilator molecule that mediates the excessive arterial vasodilatation observed in portal hypertension. The aims of this review are (1) to categorize NO synthase isoforms involved in NO overproduction; (2) to explain the mechanisms of endothelial NO synthase up-regulation; and (3) to summarize other molecules involved in the arterial vasodilatation. SN - 0192-0790 UR - https://www.unboundmedicine.com/medline/citation/17975478/The_molecules:_mechanisms_of_arterial_vasodilatation_observed_in_the_splanchnic_and_systemic_circulation_in_portal_hypertension_ DB - PRIME DP - Unbound Medicine ER -